• Tuberculosis and Respiratory Diseases
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• v.62 no.6
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• pp.499-505
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• 2007

Background: Triggering receptor expressed on myeloid cells 1 protein (TREM-1) is a cell surface molecule expressed on neutrophils and monocytes, and it plays an important role in myeloid cell-activated inflammatory response. The aim of this study was to investigate the diagnostic efficiency of soluble (s) TREM-1 in the patients who had pleural effusion from various causes. Methods: Forty-five patients with exudative pleural effusion were included in this study. The level of sTREM-1 was measured in both the serum and pleural fluids by immunoblot assay with using human-sTREM-1 antibody. Results: The pleural fluid sTREM-1 was significantly different in the three groups of exudative pleural effusion (p=0.011). Particularly, the patients with parapneumonic effusion were found to have significantly higher pleural fluid levels of sTREM-1 than patients with tuberculous (p<0.05) and malignant effusion, respectively (p<0.05). However, the serum sTREM-1 did not show a significant difference in the three groups. In order to evaluate the diagnostic utility of pleural fluid sTREM-1, the receiver operating characteristic (ROC) curve was constructed and the area under the curve (AUC) was 0.818 (p=0.001). Using a cutoff value of 103.5 pg/mL for the pleural fluid sTREM-1, the sensitivity and specificity were 73% and 81%, respectively, for differentiating parapneumonic effusion from tuberculous or malignant effusions. Conclusion: Pleural fluid sTREM-1 can be an additional marker for making the differential diagnosis of pleural effusion.

• Nutrition Research and Practice
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• v.11 no.6
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• pp.461-469
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• 2017

BACKGROUND/OBSECTIVE: Airway inflammation by eosinophils, neutrophils and alveolar macrophages is a characteristic feature of asthma that leads to pathological subepithelial thickening and remodeling. Our previous study showed that oxidative stress in airways resulted in eosinophilia and epithelial apoptosis. The current study investigated whether glutathione-containing dry yeast extract (dry-YE) ameliorated eosinophilia, goblet cell hyperplasia and mucus overproduction. MATERIALS/METHOD: This study employed $2{\mu}g$/mL lipopolysaccharide (LPS)- or 20 ng/mL eotaxin-1-exposed human bronchial epithelial cells and ovalbumin (OVA)-challenged mice. Dry-YE employed in this study contained a significant amount of glutathione (140 mg in 100 g dry yeast). RESULTS: Human bronchial epithelial cell eotaxin-1 and mucin 5AC (MUC5AC) were markedly induced by the endotoxin LPS, which was dose-dependently attenuated by nontoxic dry-YE at 10-50 ${\mu}g$/mL. Moreover, dry-YE inhibited the MUC5AC induction enhanced by eotaxin-1, indicating that eotaxin-1-mediated eosinophilia may prompt the MUC5AC induction. Oral supplementation with 10-100 mg/kg dry-YE inhibited inflammatory cell accumulation in airway subepithelial regions with a reduction of lung tissue level of intracellular adhesion molecule-1. In addition, ${\geq}50$ mg/kg dry-YE diminished the lung tissue levels of eotaxin-1, eosinophil major basic protein and MUC5AC in OVA-exposed mice. Alcian blue/periodic acid schiff staining revealed that the dry-YE supplementation inhibited goblet cell hyperplasia and mucus overproduction in the trachea and bronchiolar airways of OVA-challenged mice. CONCLUSIONS: Oxidative stress may be involved in the induction of eotaxin-1 and MUC5AC by endotoxin episode and OVA challenge. Dry-YE effectively ameliorated oxidative stress-responsive epithelial eosinophilia and mucus-secreting goblet cell hyperplasia in cellular and murine models of asthma.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.210-220
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• 1996

Background : Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. In the process of surface adherence, adhesion molecules have a clear role in intracellular signal pathway of cellular activation. Human alveolar macrophages(HAM) are frequently purified by the adherence procedure after bronchoalveolar lavage. But the experimental data of many reports about alveolar macrophages have ignored the possibility of adhesion-induced cellular activation. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be normal by chest CT. With the measurement of hydrogen peroxide release from adherent HAM to plastic surface and non-adherent HAM with or without additional stimulation of phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP), we observed the effect of the adherence to plastic surface. We also evaluated the effect of various biological surfaces on adhesion-induced activation of HAM. Then, to define the intracellular pathway of signal transduction, pretreatment with cycloheximide, pertussis toxin and anti-CD11/CD18 monoclonal antibody was done and we measured hydrogen peroxide in the culture supernatant of HAM. Results : 1) The adherence itself to plastic surface directly stimulated hydrogen peroxide release from human alveolar macrophages and chemical stimuli such as phorbol myristate acetate(PMA) or N-formyl-methionyl-leucyl-phenylalanine(fMLP) colud not increase hydrogen peroxide release in these adherent macrophages which is already activated. 2) PMA activated human alveolar macrophages irrespective of the state of adhesion. However, fMLP stimulated the release of hydrogen peroxide from the adherent macrophages, but not from the non-adherent macrophages. 3) HAM adherent to A549 cell(type II alveolar epithelium-like human cell line) monolayer released more hydrogen peroxide in response to both PMA and fMLP. This adherence-dependent effect of fMLP was blocked by pretreatment of macrophages with cycloheximide, pertussis toxin and anti-CD18 monoclonal antibody, Conclusion : These results suggest that the stimulatory effect of PMA and fMLP can not be found in adherent macrophage because of the activation of human alveolar macrophage by the adherence to plastic surface and the cells adhered to biologic surface such as alveolar epithelial cells are appropriately responsive to these stimuli. It is also likely that the effect of fMLP on the adherent macrophage requires new protein synthesis via G protein pathway and is dependent on the adhesion between alveolar macrophages and alveolar epithelial cells by virtue of CD11/CD18 adhesion molecules.

• Tuberculosis and Respiratory Diseases
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• v.43 no.6
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• pp.936-944
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• 1996

Background: Neutrophils or monocytes separated in vitro by the adherence to plastic surface are known to be activated by surface adherence itself and subsequent experimental data might be altered by surface adherence. Adhesion molecules and gene transcription of the inflammatory mediators are known to be associated in this process. To evaluate whether adhesion molecule and transcriptional activation of the inflammatory substances are also involved in the activation of human alveolar macrophage by the adherence procedure, we designed this experiment. Method : Bronchoalveolar lavage was performed in the person whose lung of either side was confirmed to be nonnal by chest cr and alveolar macrophage was harvested. To measure the expression of Interleukin-8(IL-8) mRNA, manganese superoxide dismutase(SOD) mRNA and CD11/CD18 mRNA in human alveolar macrophage of both adherence state and suspension state, Northern blot analysis was done at 0, 2, 4, 8 and 24hrs after the adherence to plastic surface and during suspension state. Then, phorbol myristate acetate(pMA) and N-formyl-methionyl-leucyl-phenylalanine(fMLP) were added respectively in the same experimental condition. Result : 1) Human alveolar macrophages in the adherent state induced IL-8 mRNA and SOD mRNA expression which was maximal at 8 hours after the adherence to plastic surface. But we could not observe the upregulation of CD18 mRNA by surface adherence. 2) PMA induced these mRNA expression both in the adherent cell and the nonadherem cells, but the induction of mRNA expression by fMLP occurred only in the adherent cells. Conclusion: These results suggest that adherence of huamn alveolar macropahge is an important cell-activating event that may play a critical role in the modulation of lung inflammatory respones.

• Journal of Veterinary Clinics
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• v.23 no.4
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• pp.393-399
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• 2006

Ketamine, one of general anesthetics for human and veterinary use, is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist which interferes with the action of excitatory amino acids. It has been reported to impair various leukocyte functions. In this study, the effect of ketamine on the oxidative burst activity (OBA) of canine peripheral blood leukocytes was examined. The OBA of canine peripheral blood phagocytes was analyzed by flow cytometry system. Ketamine at higher concentration such as $1,000{\mu}M$ exhibited a low viability of leukocytes. Thus, ketamine was used at concentration of 10 to $500{\mu}M$ showing no cytotoxic effect and high cell viability. The OBA of leukocytes in the presence or absence of latex beads was analyzed by addition of dihydrorhodamine 123. The direct treatment of ketamine revealed the inhibitory effect on the OBA of peripheral blood polymorphonuclear cells (PMN) and monocyte-rich cells but not peripheral blood mononuclear cells (PBMC) in the presence of latex beads. However, when latex beads were not added to PMN, its OBA was not inhibited by ketamine. The OBA of PMN and monocyte-rich cells but not PBMC in the presence of latex beads was also inhibited by culture supernatant from ketamine-treated- PBMC but not -PMN. But the OBA of PMN in the absence of latex beads was not inhibited by culture supernatant from PBMC treated with ketamine. Therefore, these results suggested that ketamine has the inhibitory effect on the OBA of canine peripheral blood phagocytes such as neutrophils and monocytes during phagocytic response.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.146-156
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• 2018

Spermidine is a naturally occurring polyamine compound that has recently emerged with anti-aging properties and suppresses inflammation and oxidation. However, its mechanisms of action on anti-inflammatory and antioxidant effects have not been fully elucidated. In this study, the potential of spermidine for reducing pro-inflammatory and oxidative effects in lipopolysaccharide (LPS)-stimulated macrophages and zebrafish was explored. Our data indicate that spermidine significantly inhibited the production of pro-inflammatory mediators such as nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$), and cytokines including tumor necrosis $factor-{\alpha}$ and $interleukin-1{\beta}$ in RAW 264.7 macrophages without any significant cytotoxicity. The protective effects of spermidine accompanied by a marked suppression in their regulatory gene expression at the transcription levels. Spermidine also attenuated the nuclear translocation of $NF-{\kappa}B$ p65 subunit and reduced LPS-induced intracellular accumulation of reactive oxygen species (ROS) in RAW 264.7 macrophages. Moreover, spermidine prevented the LPS-induced NO production and ROS accumulation in zebrafish larvae and was found to be associated with a diminished recruitment of neutrophils and macrophages. Although more work is needed to fully understand the critical role of spermidine on the inhibition of inflammation-associated migration of immune cells, our findings clearly demonstrate that spermidine may be a potential therapeutic intervention for the treatment of inflammatory and oxidative disorders.

• Restorative Dentistry and Endodontics
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• v.30 no.2
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• pp.138-144
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• 2005

This in vitro study monitored MMP-8 production on PMN by stimulated with the following three groups; Sonicated extracts of E. faecalis (SEF), SEF treated with $Ca(OH)_2$ (12.5mg/ml) for 7 days, and lipopolysac-charides(LPS) of E. coli. The level of MMP-8 in each group was immediately measured by ELISA. The data were analyzed with Kruskal-Wallis test and Mann-Whitney U test. In the SEF group, the level of production of MMP-8 was higher than the negative control group in low concentration ($0.05{\mu}g/ml$) of SEF (p < 0.05). but it decreased with an increase in the concentration of SEF (p < 0.05). In the case of SEF treated with $Ca(OH)_2$, all of the MMP levels were higher than negative control group (p < 0.05), but no statistical difference was found among the different SEF concentrations (p > 0.05). All of the levels in E. coli LPS were incresed with increasing concentrations (p < 0.05). According to this study we could summarized as follows: 1. MMP-8 was expressed at low level in untreated PMN group the levels of MMP-8 were upregulated in PMN stimulated by E. coli LPS groups. 2. In the SEF groups, the level of production of MMP-8 decreased with an increase in concentration of SEF (p < 0.05). So E. faecalis may have suppressive effect on the production of MMP-8 by PMN. 3. In the case of SEF treated with $Ca(OH)_2$, all of the MMP levels at different SEF concentrations were higher than untreated PMN group (p < 0.05), but no statistical difference was found among the different SEF concentrations (p > 0.05).

• Tuberculosis and Respiratory Diseases
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• v.52 no.2
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• pp.145-155
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• 2002

Background: Inflammation, where vascular endothelial cells are activated by cytokines, recruits circulating leukocytes such as neutrophils into the tissues. Mononuclear phagocytes as well as tissue cells activated by these stimuli produce these chemokines. In this study, thr effects of IL-1 and LPS on the expression of CXC chemokines such as GRO-${\alpha}$, IL-8 and ENA-78 in vascular endothelial cells and the neutrophil adhesion effects of ENA-78 and GRO-${\alpha}$ was investigated. Methods: Human umbilical vein endothelial cells were cultured and stimulated with various concentrations of IL-1 and LPS. The concentrations of the GRO-${\alpha}$, IL-8 and ENA-78 secreted were measured using enzymelinked immunosorbent assay. The effects of ENA-78 and GRO-${\alpha}$ on neutrophil adhesion to the endothelial cells were also investigated. Results: The addition of IL-1 and LPS to the vascular endothelial cells induced GRO-${\alpha}$ IL-8 and ENA-78 secretion in a time- and dose-dependent manner. The neutrophil adhesion was also increased by induction of ENA-78 and GRO-${\alpha}$ to the vascular endothelial cells in a dose-dependent manner. Conclusion: CXC chemokines such as GRO-${\alpha}$, IL-8 and ENA-78 secreted by the vascular endothelial cells play an important role in the acute inflammatory responses by stimulating neutrophil adhesion to the vascular endothelial cells, raising the possibility that the CXC chemokines are one of the targets in the clinical application of acute inflammation.

• Journal of Life Science
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• v.27 no.10
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• pp.1168-1175
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• 2017

Probiotics are usually defined as intestinal bacteria that provide healthy benefit to the host and may offer new therapeutic materials for the treatment of inflammatory diseases. Lactobacillus, Bifidobacterium and Enterococcus are known as typical probiotics. But, these bacteria have mostly a weak viability and thus decreased probiotics-mediated effects in the intestinal tract. Asthma is an inflammatory airway disease, which is characterized by the releases of inflammatory mediators including cytokine and IgE. They are mainly associated with the recruitment, activation and disregulation of specific inflammatory cells, especially mast cells, monocytes, T cells, eosinophils and neutrophils in asthma. We performed these studies as in vitro and in vivo test the human inflammatory cell lines and ovalbumin (OVA)-induced asthma mouse model. And then the inhibitory effects of Enterococcus faecalis whole extract on inflammatory responses were examined. For our examinations, the E. faecalis whole extract (Ef extract) was acquired from whole bacteria of E. faecalis using freeze/thawing after ultrasonication method. As results, OVA-mediated THP-1 cell viability was decreased by the treatment of Ef extract. In the asthmatic mouse model, Ef extract inhibited the infiltration of inflammatory cells into the inflammatory sites and blood. This whole extract may have anti-asthmatic effects associated with the regulation of IL-5 and IgE expression. It may also be a promising candidate in anti-allergic medicine for the treatment of asthma.

• Journal of Chest Surgery
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• v.36 no.12
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• pp.894-903
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• 2003

Protection against ischemia-reperfusion injury is crucial for successful transplantation of the lung. It has been known that nitric oxide has many favorable effects on the donor lungs but at the same time, has some potential side effects of cytotoxicity. In this regards, we investigated whether the administration of nitroglycerin could decrease ischemia-reperfusion injury in isolated rat lung reperfusion model for the confirmation of the effect of nitroglycerin, a donor of nitric oxide, on lung transplantation. Material and Method: 35 Sprague-Dawley species male white rats were used for this experiment. For nitroglycerin group (n=18), nitroglycerin was administered intravenously followed by mixed in flushing solution for preservation. As a control group (n=17), we used the same amount of normal saline. To evaluate the effect of nitroglycerin on the lung, heart-lung block was obtained, weighed and stored in University of Wisconsin Solution at 1$0^{\circ}C$ for 24 hours. In each group of the isolated lungs, reperfusion was carried out with Krebs-Hensleit-diluted human blood for 60 minutes. As parameters of the state of the isolated lung, peak inspiratory and pulmonary arterial pressures were continuously recorded. Oxygen and carbon dioxide tension of reperfusing blood were measured before and after 30, 60 minutes of reperfusion. After sixty minutes of reperfusion, protein content in bronchoalveolar lavage fluid was measured also for the evaluation of the degree of alveolar flooding. Lung myeloperoxidase activity was determined to verify the accumulation of neutrophils. Results: Although statistically significant differences were not noted in peak inspiratory and pulmonary arterial pressure between control and nitroglycerin group, latter group showed lowering tendency of pulmonary arterial pressure during the entire reperfusion period. Oxygen tension was higher (p<0.05) in nitroglycerin group compared with that of the control group, in contrast, there were no differences in carbon dioxide tension, protein content in bronchoalveolar lavage fluid and myeloperoxidase activity between the groups. In the examination of ultrastructural changes, nitroglycerin denoted the protective effect on the pulmonary architecture compared with that of control group. Conclusion: Collectively, on the bases of these experimental results, prior treatment of donor lung with nitroglycerin could result in better preservation of the lung. Consequently, these nitroglycerin preserved lungs are thought to be more suitable for successful transplantation of the lung.